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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The body temperatures of mature lean and obese C57BL/6J mice were measured just after feeding, during ad libitum access to food, or every 24 h throughout a 3-day fast. Obese mice had body temperatures 1.0-1.4 degrees C lower than lean mice in the postprandial state and during ad libitum feeding. During food deprivation, obese mice became more hypothermic than lean sex-matched controls. A 5 degrees C fall in body temperature was observed in mutant females in the first 24 h of starvation, about twice that seen in any other experimental group. Over the same period the temperature changes of obese males and lean females were similar and both groups had larger hypothermic responses than lean males. The present results indicate that both genotype and gender affect thermoregulation in these mice. Under normal colony room conditions (ad libitum feeding, 23 degrees C) the ob/ob mutation is expressed by lower body temperatures which along with hypoactivity and hyperphagia account for the high rates of energy storage. When food availability is limited, females of both phenotypes display an increased capacity to reduce their maintenance energy requirements by lowering body temperatures. This hypothermia may be responsible for both the increased conservation of body mass seen during starvation and the slightly greater (5%) fat stores observed in female mice.
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PMID:Fed and fasting thermoregulation in ob/ob mice. 406 46

Twenty-five patients suffering from gross refractory obesity agreed to be starved in hospital until they weighed not more than 25% over their ideal weight. Two discharged themselves prematurely, four defaulted from follow-up, and seven who for various reasons were discharged before completing their treatment have since regained weight. After a mean follow-up period of nearly 18 months 8 of the remaining 12 remained near their weight on discharge. Some kind of initial psychological assessment might improve these results, but prolonged therapeutic starvation may be of value in young patients with gross refractory obesity who are psychologically suitable and socially able to undergo such treatment.
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PMID:Further experience with prolon- ged therapeutic starvation in gross refractory obesity. 549 Dec 55

1. The specific activity of ATP citrate lyase is two to four times as great in livers of mice with hereditary obesity as in livers of their non-obese siblings. The enzyme activity in both types of mice can be reduced by starvation, and can be increased by refeeding starved animals. The specific activity of acetyl-CoA synthetase is approximately the same in both types of mice. 2. ATP citrate lyase of mammary gland of the rat undergoes large increases in activity after the onset of lactation. It declines rapidly upon weaning. 3. The changes in activity of ATP citrate lyase in obesity and lactation are consistent with the hypothesis that the enzyme supplies extramitochondrial acetyl-CoA for fatty acid synthesis.
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PMID:Citrate and the conversion of carbohydrate into fat. Citrate cleavage in obesity and lactation. 596 97

We have studied the effects of starvation and of obesity on somatostatin, insulin, and glucagon release from an isolated perfused organ system in fed and 3- and 5-day fasted Holtzman rats and in obese (fa/fa) and lean (Fa/?) Zucker rats. Fasting for 3 days significantly decreased basal (-71%) and amino acid-stimulated (-62%) somatostatin output. After 5 days of starvation, there was a significant increase over the 3-day level in somatostatin output stimulated by amino acid plus glucose (+540%) and by amino acids plus tolbutamide (+238%). Three and five days of starvation severely depressed insulin output while having no statistically significant effects on glucagon secretion. Somatostatin output from obese Zucker rats was significantly greater than that from lean controls in response to amino acids (41.2 +/- 13.2 vs. 16.3 +/- 10.3 ng/25 min, P less than 0.05). Insulin output was greatly increased from obese compared to lean Zucker rats, whereas there were no statistically significant differences in glucagon output. These data show that fasting decreases and obesity increases both somatostatin and insulin release. They suggest that altered stimulation by nutrients was primarily responsible for changes in somatostatin and insulin release observed in starving and obese rats.
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PMID:Effects of starvation and obesity on somatostatin, insulin, and glucagon release from an isolated perfused organ system. 611 33

Normal, male Sprague-Dawley (S-D) rats and female, lean and obese Zucker rats were studied in the fed state and after 48 hours of food deprivation. Somatostatin-like immunoreactivity (SLI) was measured from acetic acid extracts of oesophagus-cardia, stomach, small and large intestine, pancreas, hypothalamus, pituitary and cerebellum. Within the CNS, the highest levels of SLI were found in the hypothalamus, while in the gut, these levels were highest in the stomach and pancreas. All Zucker rats displayed higher hypothalamic levels of SLI than did S-D rats. Obese Zucker rats in the fed state differed from their lean littermates in that SLI levels were lower in oesophagus-cardia, stomach and hypothalamus, while being higher in pancreas and pituitary. The response to starvation in both obese and lean Zucker rats was qualitatively similar, and included significant increases in stomach and oesophagus-cardia SLI, but with a significant fall hypothalamic SLI. We have concluded that the increase in gastrointestinal SLI with starvation in Zucker as well as in S-D rats may represent a significant regulatory mechanism in nutrient homeostasis. We postulate that gastric SLI may decrease the availability of intestinal insulin secretagogues in the fasting state. This adaptive mechanism appears to be intact in the obese Zucker rat.
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PMID:Starvation increases gastrointestinal somatostatin in normal and obese Zucker rats: a possible regulatory mechanism. 612 4

1. The effects of food intake and the fatty acid composition of the diet on the hepatic stearoyl-CoA desaturase activity of obese-hyperglycaemic (ob/ob) mice were investigated. 2. Obese mice fed on a commercial mouse diet, ad libitum, had 6.5-fold more activity per liver cell than had lean mice. 3. On a diet containing 14% corn oil the activity was 65% less in obese mice and 62% less in lean mice compared with animals fed on the commercial diet. 4. Feeding with 14% saturated fat in the diet doubled the activity in lean mice compared with those on the commercial diet, but had no effect on the activity in obese mice. 5. Obese mice fed on the corn-oil diet contained a higher proportion of linoleic acid in the liver lipids than did lean mice fed on the commercial diet, but the acyl-CoA desaturase activity was 125% higher than in the lean mice. 6. Limiting the food intake of obese mice by pair-feeding with lean mice decreased their acyl-CoA desaturase activity when the animals were fed on the saturated-fat diet, but the activity remained 75% higher than in lean mice, whereas in obese mice pair-fed on the corn-oil diet the activity was the same as in lean mice. 7. During starvation the acyl-CoA desaturase activity in livers from obese mice decreased more slowly and proportionately less than in livers from lean mice. 8. It is concluded that increased substrate supply as a result of hyperphagia and not low concentration of linoleic acid is the main factor causing high acyl-CoA desaturase activity in obese mice.
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PMID:The regulation of hepatic stearoyl-coenzyme A desaturase in obese-hyperglycaemic (ob/ob) mice by food intake and the fatty acid composition of the diet. 612 73

Obesity was induced in male Sprague-Dawley rats by overfeeding a cafeteria-style diet. The obesity was characterized by both adipocyte hypertrophy and hyperplasia. Body weight was then reduced by starvation to match that of control animals that had been fed ordinary Purina Chow. The previously obese rats were then refed to match the same body weight as controls, or given the same amount of Purina Chow as consumed by the controls. This resulted in a remaining moderate obesity, now due only to adipocyte hyperplasia with normal fat cell size. The previously obese rats needed less energy to keep their body weight equal to controls, and they spontaneously ate less than controls. They were, however, less food efficient because they did not accumulate as much energy in fat and protein depots during the period of refeeding as the controls did, and consequently must have transformed more energy into heat. This is in sharp contrast to nonobese animals subjected to a similar experimental procedure. Lipogenic enzymes and lipoprotein lipase activity in adipose tissue as well as plasma insulin concentrations were elevated in overfed rats but normalized during refeeding of Chow after fasting.
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PMID:Refeeding after fasting in the rat: effects of dietary-induced obesity on energy balance regulation. 633 94

The basal rate of lipolysis and basal lipoprotein lipase activity were determined in vitro in subcutaneous adipose tissue obtained from eight healthy non-obese subjects, ten obese subjects before and during one week's starvation, nine untreated non-insulin dependent diabetics and seven treated non-insulin dependent diabetics whose disease had been under metabolic control for at least three months. There was a negative correlation between the rate of lipolysis and activity of lipoprotein lipase in untreated diabetes mellitus and during starvation (r from -0.87 to -0.81). Under these two conditions the rate of lipolysis is increased and the lipoprotein lipase activity is decreased. There was no correlation between lipolysis and lipoprotein lipase in non-obese subjects, non-starving obese subjects and treated diabetic patients (r from 0.11 to 0.36). Thus, during starvation and in untreated diabetes, there is a strong reciprocal relationship between basal lipolytic activity and basal lipoprotein lipase activity in human adipose tissue which is not found under normal conditions or in obesity and well-controlled diabetes. It is concluded that a negative connection between lipolysis and lipoprotein lipase in human adipose tissue may be of physiological importance for the regulation of the energy balance in conditions such as untreated non-insulin dependent diabetes and starvation where adipose tissue lipids are the major source of energy.
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PMID:The relationship between the basal lipolytic and lipoprotein lipase activities in human adipose tissue. 634 23

Insulin resistance is found in physiological (starvation, gestation) or pathological (diabetes, obesity, uremia, cortisol or growth hormone excess) situations. In order to study insulin resistance, a number of tests have been developed which have evolved in term of practical and conceptual complexity. In the present paper, these tests are analyzed for their reliability in answering the following questions: does an insulin resistance exist? Is it possible quantify it? What are the causes (receptor or post receptor defect) and the tissues producing or utilizing glucose involved in insulin resistance? Emphasis is placed upon a newly developed technique: the euglycemic, hyperinsulinemic glucose clamp. Progress in the knowledge of insulin resistance as well as the problems or limitations linked to this latter technique are discussed.
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PMID:[Technics for studying insulin resistance in vivo]. 639 95

The kinetics of acetoacetate (A) and beta-hydroxybutyrate (B) have been studied following the injection as a pulse or continued infusion of [3-14C]acetoacetate (A*) or [14C]beta-hydroxybutyrate (B*) into six newly diagnosed, untreated, ketotic diabetic patients, ten obese subjects in the postabsorptive state, and the ten obese subjects after 1-2 weeks starvation (50 cal per day). Employing a compartmental model of acetoacetate and beta-hydroxybutyrate kinetics developed using CONSAM for normal subjects, the rate coefficients (Lij), rates of release of newly synthesized acetoacetate and beta-hydroxybutyrate into the blood (UA, UB), and fractional removal of each compound (FCRA and FCRB) were calculated. Ketone body release into blood (UA + UB) in diabetic subjects was threefold higher than normal (mean +/- SD, 208 +/- 118 versus 81 +/- 66 mumol min-1 m-2) and in obese subjects the rate increased on starvation from 171 +/- 70 to 569 +/- 286 mumol min-1 m-2. In each case most of the increase was in beta-hydroxybutyrate. The major change in diabetes and on starvation of the obese subjects was in the rate coefficient for removal of ketone bodies. Normally 0.168 +/- 0.109 min-1, it was 0.055 +/- 0.040 min-1 in the diabetic patients and fell from 0.066 +/- 0.040 to 0.027 +/- 0.019 min-1 in the obese subjects on starvation. In normal subjects, FCRA was similar to FCRB (0.226 +/- 0.142 versus 0.188 +/- 0.124 min-1). However, in diabetics, FCRA was 0.074 +/- 0.044 and FCRB was 0.050 +/- 0.034 min-1 and both were lower than normal. On starvation of obese subjects, FCRA fell from 0.199 +/- 0.047 to 0.089 +/- 0.035 min-1, whereas FCRB fell from 0.141 +/- 0.040 to 0.033 +/- 0.012 min-1. Therefore, the removal of beta-hydroxybutyrate was impaired more than that of acetoacetate in all patients. Our results confirm previous observations that ketosis is associated with high rates of ketogenesis and a decrease in fractional clearance. In addition, we found that in diabetes, obesity, and in obese subjects following starvation, most of the increased synthesis was in beta-hydroxybutyrate and that the clearance of beta-hydroxybutyrate decreased more than that of acetoacetate.
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PMID:Ketone body kinetics in humans: the effects of insulin-dependent diabetes, obesity, and starvation. 644 Sep 41


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